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Cited by 222Dementia and Cognitive Impairment ResearchAlzheimer's disease research and treatmentsMedical Imaging Techniques and Applications

Diagnostic Performance of RO948 F 18 Tau Positron Emission Tomography in the Differentiation of Alzheimer Disease From Other Neurodegenerative Disorders

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Leuzy, Antoine, Smith, Ruben, Ossenkoppele, Rik, Santillo, Alexander, Borroni, Edilio, Klein, Gregory, Ohlsson, Tomas, Jögi, Jonas +5 more·2020·JAMA Neurology
DOI 10.1001/jamaneurol.2020.0989PMC PMC7215644
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Abstract

Importance: The diagnostic performance of second-generation tau positron emission tomographic (PET) tracers is not yet known. Objective: To examine the novel tau PET tracer RO948 F 18 ([18F]RO948) performance in discriminating Alzheimer disease (AD) from non-AD neurodegenerative disorders. Design, Setting, and Participants: In this diagnostic study, 613 participants in the Swedish BioFINDER-2 study were consecutively enrolled in a prospective cross-sectional study from September 4, 2017, to August 28, 2019. Participants included 257 cognitively unimpaired controls, 154 patients with mild cognitive impairment, 100 patients with AD dementia, and 102 with non-AD neurodegenerative disorders. Evaluation included a comparison of tau PET tracer [18F]RO948 with magnetic resonance imaging (MRI) and cerebrospinal fluid and a head-to-head comparison between [18F]RO948 and flortaucipir F 18 ([18F]flortaucipir) in patients with semantic variant primary progressive aphasia (svPPA). Exposures: [18F]RO948 (all patients) and [18F]flortaucipir (3 patients with svPPA) tau PET; MRI (hippocampal volume, composite temporal lobe cortical thickness, whole-brain cortical thickness) and cerebrospinal fluid measures (p-tau181 and amyloid Aβ42 and Aβ40 ratio[Aβ42/Aβ40], and Aβ42/p-tau181 ratio). Main Outcomes and Measures: Standard uptake value ratios (SUVRs) in 4 predefined regions of interest (ROIs) reflecting Braak staging scheme for tau pathology and encompass I-II (entorhinal cortex), III-IV (inferior/middle temporal, fusiform gyrus, parahippocampal cortex, and amygdala), I-IV, and V-VI (widespread neocortical areas), area under the receiver operating characteristic curve (AUC) values, and subtraction images between [18F]RO948 and [18F]flortaucipir. Results: Diagnostic groups among the 613 participants included cognitively unimpaired (mean [SD] age, 65.8 [12.1] years; 117 men [46%]), mild cognitive impairment (age, 70.8 [8.3] years; 82 men [53%]), AD dementia (age, 73.5 [6.7] years; 57 men [57%]), and non-AD disorders (age, 70.5 [8.6] years; 41 men [40%]). Retention of [18F]RO948 was higher in AD dementia compared with all other diagnostic groups. [18F]RO948 could distinguish patients with AD dementia from individuals without cognitive impairment and those with non-AD disorders, and the highest AUC was obtained using the I-IV ROI (AUC = 0.98; 95% CI, 0.96-0.99 for AD vs no cognitive impairment and AUC = 0.97; 95% CI, 0.95-0.99 for AD vs non-AD disorders), which outperformed MRI (highest AUC = 0.91 for AD vs no cognitive impairment using whole-brain thickness, and AUC = 0.80 for AD vs non-AD disorders using temporal lobe thickness) and cerebrospinal fluid measures (highest AUC = 0.94 for AD vs no cognitive impairment using Aβ42/p-tau181, and AUC = 0.93 for AD vs non-AD disorders using Aβ42/Aβ40). Generally, tau PET positivity using [18F]RO948 was observed only in Aβ-positive cases or in MAPT R406W mutation carriers. Retention of [18F]RO948 was not pronounced in patients with svPPA, and head-to-head comparison revealed lower temporal lobe uptake than with [18F]flortaucipir. Conclusions and Relevance: In this study, elevated [18F]RO948 SUVRs were most often seen among Aβ-positive cases, which suggests that [18F]RO948 has high specificity for AD-type tau and highlights its potential as a diagnostic marker in the differential diagnosis of AD.

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  • Structural MRI represents a relatively lower-cost alternative to spatially measure in vivo neurodegeneration, but it is substantially less specific to AD pathology compared to PET.

    “Structural magnetic resonance imaging (MRI) represents a relatively lower‐cost alternative to spatially measure in vivo neurodegeneration, but it is substantially less specific to AD pathology compared to PET. 5 , 6 , 7 , 8”

    From Machine learning prediction of tau‐PET in Alzheimer's disease using plasma, MRI, and clinical data (2025) · cites this paper as [6]

    The Discussion (page unavailable) says MRI-based atrophy measures track disease progression and that MRI performed less well than [18F]RO948 tau PET in distinguishing AD dementia from non-AD disorders. It does not address MRI’s relative cost, and its comparison of diagnostic performance does not establish specificity to AD pathology itself. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • These biomarkers (t-tau and p-tau) remain at normal concentrations in other neurodegenerative disorders with substantial neurodegeneration, and also those with tau pathology.

    “However, these biomarkers remain at normal concentrations in other neurodegenerative disorders with substantial neurodegeneration,8, 9, 10 and also those with tau pathology.11, 12, 13”

    From Cerebrospinal fluid p-tau231 as an early indicator of emerging pathology in Alzheimer's disease (2022) · cites this paper as [12]

    The Introduction (page unavailable) says that tau pathology occurs in non-Alzheimer neurodegenerative disorders, and the Conclusions (page unavailable) discuss the diagnostic performance of CSF p-tau181. Neither passage establishes that CSF t-tau and p-tau remain at normal concentrations in those disorders, including those with tau pathology. Searches for their concentrations in non-Alzheimer disorders did not find that result in our copy. (LLM, conf=0.73)

    Experimental — accuracy not yet measured

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Authors
Leuzy, A., Smith, R., Ossenkoppele, R., Santillo, A., Borroni, E., Klein, G., Ohlsson, T., Jögi, J., Palmqvist, S., Mattsson-Carlgren, N., Strandberg, O., Stomrud, E., & Hansson, O.
Affiliations
  • Lund University (SE)
  • Skåne University Hospital (SE)
  • F. Hoffmann-La Roche AG (CH)
  • Clinical Memory Research Unit, Department of Clinical Sciences, Lund University, Malmö, Sweden
Corresponding author
  • Leuzy, Antoine
  • Hansson, Oskar
ORCID
Venue
JAMA Neurology
Publisher
American Medical Association (AMA)
Published
2020-08-01
Volume
77
Issue
8
Pages
955
ISSN
2168-6149 (ISSN-L)
DOI
10.1001/jamaneurol.2020.0989
PMC
PMC7215644
OpenAlex
W3021135759
Cited by
222
References
14
Citations by year
2026: 24 · 2025: 35 · 2024: 33 · 2023: 29 · 2022: 38 · 2021: 44 · 2020: 18
FWCI
23.53
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • JAMA Neurology (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • Amsterdam UMC (VU Amsterdam) - Institutional Repository (publishedVersion, other-oa)
  • Lund University Publications (Lund University) (submittedVersion)
  • Data Archiving and Networked Services (DANS) (submittedVersion, other-oa)
Funders
  • Knut och Alice Wallenbergs Stiftelse
  • Vetenskapsrådet
  • Marcus och Amalia Wallenbergs minnesfond
Topics
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Medical Imaging Techniques and Applications
Keywords
Alzheimer's disease, tau PET, 18F-flortaucipir, semantic dementia, Braak staging, p-tau181, amyloid biomarkers, mild cognitive impairment, diagnostic accuracy, neurodegeneration biomarkers, cerebrospinal fluid biomarkers
MeSH terms
Adult, Aged, Aged, 80 and over, Alzheimer Disease, Cerebral Cortex, Cross-Sectional Studies, Diagnosis, Differential, Female, Fluorine Radioisotopes, Humans, Male, Middle Aged, Sweden, tau Proteins, Magnetic Resonance Imaging, Cine, Neurodegenerative Diseases, Positron-Emission Tomography, Cognitive Dysfunction, White Matter

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